Pairings of light and rotation result in a long-term suppression of phototaxic behavior for the mollusc Hermissenda. Two K+ currents in Hermissenda Type B photoreceptors (IA and IK-Ca) are reduced, and a calcium current (ICa) is enhanced, by associative training. Type A photoreceptor light responses are also changed and increases in a K current (IK-Ca) may be responsible. These long-lasting changes in ionic conductances comprise a biophysical basis for long-term information storage. We propose to study the cellular mechanisms by which these long term ionic current changes occur, and in particular the roles that serotonin (5-HT) and protein kinase C (PKC)-activation may play. We will condition the isolated nervous system of Hermissenda using a protocol which preserves the normal synaptic input to Type B cells (intact synapses protocol). Current-clamp and two-electrode voltage clamp techniques will be used to determine the ionic basis of short-term training-produced changes in Type B cells: cumulative depolarization and decreased membrane conductance. The role of PKC-dependent and calcium/calmodulin-dependent phosphorylation pathways in these changes will be assessed. We shall study the gating, permeation, pharmacology, and possible phosphorylational control of K+ channels from Hermissenda Type B cells through, single channel measurements of ion fluxes, and will determine the ability of protein kinase C to modify K+ channel properties.